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CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

ABSTRACT: In this experiment we in vitro activated CLL cells on a layer of fibroblasts expressing CD40L (3T40) or nothing (3T3) for 48 hours. After the 48 hours, cells were taken off the fibroblasts and sorted for viable CD19+ cells. Then we performed RNA sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201341 | GEO | 2022/05/20

REPOSITORIES: GEO

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CD40 stimulation + dasatinib treatment of chronic lymphocytic leukemia (CLL) cells

Project description:In this experiment we in vitro activated CLL cells on a layer of fibroblasts expressing CD40L (3T40) in the presence of 100 nM Dasatinib for 48 hours. After the 48 hours, cells were taken off the fibroblasts and sorted for viable CD19+ cells. Then we performed RNA sequencing.

2024-05-01 | GSE264554 | GEO

CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

Project description:In this experiment we in vitro activated T cells from CLL patients either in the presence or absence of their autologous CLL cells. After 48 hours of antiCD3/antiCD28 stimulation, the CD4 cells were FACS sorted from two condition and RNA sequencing was performed on these cells.

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miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples.

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miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

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2015-06-15 | E-GEOD-62137 | biostudies-arrayexpress

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

2014-10-06 | GSE55288 | GEO

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

Project description:Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 ÂµM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-Î± 23 CLL patients (10 Pre samples, 23 Ctrl samples, 23 IL-4 samples, 1 IL-4 plus ERK inhibitor sample, 1 IL-4 plus NFkB inhibitor sample, 1 IL-4 plus Pifithrin sample), 13 NBC (10 Pre samples, 10 Ctrl samples, 13 IL-4 samples)

2014-10-06 | E-GEOD-55288 | biostudies-arrayexpress

CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

Project description:CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

| PRJNA830901 | ENA

Gene signature of CLL cells cultured with activated T cells or CD40L-expressing cells

Project description:Chronic Lymphocytic Leukemia (CLL) cells multiply in secondary lymphoid tissue but the mechanisms leading to their proliferation are still uncertain. In addition to BCR-triggered signals, other microenvironmental factors might well be involved. In proliferation centres, leukemic B cells are in close contact with CD4+CD40L+Â T cells. Therefore, we here dissected the signals provided by autologous activated T cells (Tact) to CLL cells. Although the gene expression profile induced by Tact was highly similar to that induced by sole CD40 signaling, an obvious difference was that Tact induced proliferation of CLL cells. We determined that stimulation with only CD40L+IL-21 was sufficient to induce robust proliferation in CLL cells. We then defined an IL-21-induced gene signature in CLL, containing components of JAK-STAT and apoptosis pathways, and this signature could be detected in lymph node (LN) samples from patients. Finally, we could detect IL-21 RNA and protein in LN, and IL-21 productionÂ ex vivoÂ by LN CD4+CXCR5+ follicular helper T cells. These results indicate that, in addition to BCR signaling, activated T cells might contribute to CLL cell proliferation via CD40 and IL-21. Targeting these signaling pathways might offer new venues for treatment of CLL.Â CLL cells were cultured under different conditions for 16 hours and then sorted to purity as CD20+ CD5+ cells.

2013-10-07 | E-GEOD-50572 | biostudies-arrayexpress

Temporal transcriptional response from primary human chronic lymphocytic leukemia (CLL)-cells after B-cell receptor stimulation.

Project description:The B-cell receptor (BCR) signaling is crucial for the pathophysiology of most leukemias and lymphomas originated from mature B lymphocytes and has emerged as a new therapeutic target, especially for chronic lymphocytic leukemia (CLL). However, the precise mechanisms by which BCR signaling controls neoplastic B-cell proliferation are ill characterized. This work was performed using primary leukemic cells of untreated patients at initial stage of CLL (Binet stage A / Rai 0) presenting biological characteristics of aggressive form of the disease (unmutated IGHV genes and ZAP70 protein expression). In order to mimic the primary leukemogenic step occurring in vivo, this study focused on the BCR-dependent proliferation of CLL cells induced ex vivo using anti-IgM, together with mandatory co-stimulating factors (CD40L, IL-4 and IL-21) (Schleiss, Sci Rep, 2019). Cell proliferation was objectivized by the emergence of proliferative clusters and the presence of more than 25% of CLL cells that did undergo division within the cell culture at day 6. To capture the specific actors of the proliferative response in these samples, we also included non-proliferating control CLL samples. Gene expression was analyzed by RNA-seq before stimulation (T0) and at the time points 1h, 1h30, 3h30, 6h30, 12h, 24h, 48h and 96h after cell stimulation (n=54 data points), the latest time points corresponding to the emergence of the proliferation clusters.

2021-05-12 | GSE130385 | GEO

The Proteome Landscape of Chronic Lymphocytic Leukemia (CLL)

Project description:Many functional consequences of mutations on tumor phenotypes in chronic lymphocytic leukemia (CLL) are only partially known. This is in part due to a scarcity of information on the proteome of CLL. We profiled the proteome of 117 CLL samples with data-independent acquisition mass spectrometry (DIA-MS) and integrated the results with genomic, transcriptomic, functional data and clinical outcome. We found trisomy 12 and IGHV to be major determinants of proteome variation in CLL (1055 and 542 differential proteins FDR of 5%). Trisomy 12 was associated with limited protein abundance buffering. Protein complex analyses detected functional units involved in BCR/PI3K/AKT signaling in CLL with trisomy 12. We associated protein expression with response to anticancer drugs, and STAT2 protein expression emerged as a biomarker for the prediction of response to kinase inhibitors including BTK and MEK inhibitors. STAT2 protein levels were determined by gene dosage (trisomy 12), stabilization in a protein complex and linked to interferon signaling in CLL. This study highlights the emerging importance of protein abundance profiling in CLL biology.

2021-09-24 | PXD022198 | Pride

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